Abstract
Lack of insight into the mechanisms underlying hepatocellular carcinoma (HCC) metastasis has hindered the development of curative treatments. Overexpression of interleukin‐13 receptor alpha 2 (IL13RA2) has been reported to contribute to invasion and metastasis in several tumors. However, the role of IL13RA2 in HCC remains to be characterized. In this study, we identified that low expression of IL13RA2 is associated with poor survival of patients with HCC, and demonstrated that IL13RA2 knockdown endows HCC cells with invasive potential. Mechanistically, silencing of IL13RA2 promotes partial epithelial‐mesenchymal transition via increasing extracellular signal‐regulated kinase phosphorylation in HCC. Collectively, our results suggest that IL13RA2 may have potential as a prognostic biomarker for HCC.
Highlights
Up to 2018, hepatocellular carcinoma (HCC) was evaluated as the sixth most common cancer in the world and the fourth leading cause of cancer death [1]
Compared with most HCC cell lines (Hep G2, PLC/ PRF/5, SMMC7721, Huh7), the mRNA expression of Interleukin-13 receptor alpha 2 (IL13RA2) was slightly higher in hepatocyte L02 (Fig. 2B,C), which was analogous to The Cancer Genome Atlas (TCGA) analysis result
In HCCLM3 cells, IL13RA2 silencing up-regulated the expression of N-cadherin and Vimentin, with no obvious change in Ecadherin. These results demonstrated that IL13RA2 knockdown HCC cells underwent different types of epithelial-mesenchymal transition (EMT) program
Summary
Up to 2018, hepatocellular carcinoma (HCC) was evaluated as the sixth most common cancer in the world and the fourth leading cause of cancer death [1]. The metastasis and recurrence of HCC are a major obstacle to improving overall survival (OS) and quality of life of patients. The mechanisms underlying the metastasis of HCC remain obscure, leading to limited metastasis-targeted therapeutics. Genetic and epigenetic changes that form networks or pathways are involved in the whole metastatic process. Interleukin-13 receptor alpha 2 (IL13RA2), 43 kDa, is one of the receptors for IL-13 [5]. The classic pathway for IL-13 activation is JAK/STAT6 via binding to receptor interleukin-13 receptor alpha 1, not IL13RA2.
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